Vascular endocan (ESM-1) is markedly overexpressed in clear cell renal cell carcinoma

Histopathology. 2010 Jan;56(2):180-7. doi: 10.1111/j.1365-2559.2009.03458.x.

Abstract

Aims: In kidney cancer, new anti-angiogenic therapies have emerged requiring parameters of effectiveness. The aim was to analyse the expression of endocan or endothelial cell-specific molecule-1, which is a proteoglycan up-regulated in presence of pro-angiogenic factors.

Method and results: We investigated 44 renal clear cell carcinomas (RCC) and 25 papillary carcinomas (PC). Circulating endocan was detected by enzyme-linked immunosorbent assays (ELISA) in 14 patients with RCC, in eight with PC and in 15 healthy volunteers. Endocan was detected by immunohistochemistry in endothelial cells in almost all the cases of RCC without immunoreactivity in tumour cells. In PC, only 5/25 tumours exhibited weak immunoreactivity. Reverse transcriptase-polymerase chain reaction study confirmed that endocan levels were strongly increased in RCC. Endocan was also detected by ELISA at levels from 3- to 10-fold higher in the sera of patients with RCC. In vitro, addition of sunitinib prevented the release of endocan in human umbilical vascular endothelial cells when induced by vascular endothelial growth factor.

Conclusions: Our results showed that endocan is overexpressed in patients with RCC. Endocan could therefore appear as a marker of interest in the follow-up and may be a potential parameter to monitor the tumour response to anti-angiogenic therapeutics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inducing Agents / pharmacology
  • Angiogenesis Inhibitors / pharmacology
  • Carcinoma, Renal Cell / genetics*
  • Carcinoma, Renal Cell / metabolism
  • Carcinoma, Renal Cell / pathology
  • Cells, Cultured
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Humans
  • Indoles / pharmacology
  • Kidney Neoplasms / genetics*
  • Kidney Neoplasms / metabolism
  • Kidney Neoplasms / pathology
  • Neoplasm Proteins / blood
  • Neoplasm Proteins / genetics*
  • Proteoglycans / blood
  • Proteoglycans / genetics*
  • Pyrroles / pharmacology
  • Sunitinib
  • Umbilical Cord / cytology
  • Vascular Endothelial Growth Factor A / pharmacology

Substances

  • Angiogenesis Inducing Agents
  • Angiogenesis Inhibitors
  • ESM1 protein, human
  • Indoles
  • Neoplasm Proteins
  • Proteoglycans
  • Pyrroles
  • Vascular Endothelial Growth Factor A
  • Sunitinib